Tuesday, December 16, 2014

Not the Bees!

By MB

It is
an uncomfortable fact to consider that parasites may be the predominant life
form on Earth, perhaps even outnumbering free-living species by 4-to-12.
It is fortunate then that most parasites exist in a specific niche, only able
to parasitize an individual species or a small number of closely related
species2. This drives an evolutionary war of sorts, where parasites
infect a host population, hosts adapt and send on their genes to offspring,
prompting the parasite to respond in turn by improving their parasitizing
ability. This gives the host an array of defenses against that specific
parasite, but unfortunately that's not always enough. Sometimes the niche
occupied by a parasite can be usurped by another, leaving the host to the whims
of this new invader. Enter Nosema ceranae,
a unicellular parasite that did just that by jumping from the eastern honey bee
(Apis nosema) to the western one (Apis mellifera)4.Ecologically
speaking it happened in the blink of an eye, and the consequences have been
disastrous.

In
2006 and 2007 western honey bee colonies seemed to be disappearing over night,
and even those that survived suffered abnormally high levels of attrition
following the winter months. This phenomenon was given the label Colony
Collapse Disorder (CCD), and has led to a loss of around 34% of the bee
population yearly from 2007 to 20103. There is no one cause to CCD,
usually being a combination of circumstances7, but a factor common
to many cases is the presence of N.
ceranae5. The timeline of N.
ceranae switching hosts matches events leading up to the large incidence of
CCD. Before N. ceranae's jump N. apis was found globally in A. mellifera
populations, but post jump it has beenlargely displaced becoming limited to northern and western Europe5.
Not much is known about how the organism made the jump, but researchers have
put the time of the jump somewhere between a decade and two decades ago5,
which falls in line with the beginning of the bee die off we are currently
experiencing.

N. ceranae's
effectiveness against A. mellifera is two-fold: First because it jumped
from a closely related species it is already effective at co-opting metabolic
proteins, and second the infection interferes not only on a physiological level
but a behavioral level as well. Bee's collecting pollen can also ingest Nosema
spores, and when they return to the colony the spores can spread among the
population of bees. This spread was exacerbated by humans, with the accidental
transport of infected bees by commercial and hobbyist beekeepers5.
Once a bee has ingested some spores the fungi will move to and infect the cells
of the midgut, where it proliferates8. The midgut proves to be an
ideal environment for the parasite, as it is able to absorb the nutrients it
needs to survive right at the source of where the bee breaks down nectar into
sugar. Although the mechanism for how it is able to accomplish this is unknown,
the parasite further capitalizes on its location by actively suppressing
proteins in the bee that utilize or store sugars, and increasing the expression
of proteins involved in carbohydrate catabolism8. This creates a
dangerous feedback loop for the bee because it will breakdown carbohydrates for
sugar to sate its hunger, but being unable to use or store it will continue to
breakdown more and more food. Left unchecked this has further consequences
impacted not just the infected bee, but also healthy bees within the colony.

Normally bees are very social
creatures, and returning foragers share the food that they collect with the
colony6. Infected bees however, both demonstrate a greater
inclination to taking in food stocks from the hive and are much less likely to
share collected resources6. While perhaps unsurprising this
behavioral change may be the largest contributor to how N. ceranae
influences CCD. Because infected bees want to take in more food sources they
will spend more time where the food in the hive is, leaving spores to the
fungus there(Nosema is orally ingested contributing to infection in the
hive). A second issue is that CCD is most prevalent in the winter when bees
don't have access to food sources and must rely on what was stored. Infected
bees consume more, to compensate for their hunger, and in turn contribute to
winter starvation possibly dooming the colony.

Certainly this parasitic jump
has been awful for global A. mellifera populations, but from the
perspective of you are I a fair question remains: so what, who cares? Beyond
the obvious association to honey production, the western honey bee has an
enormous economic role in agriculture7. They are by and large the
largest pollinators in nature3, and up to a third of the food we eat
is pollinated by bees9. If A. mellifera were to go extinct
the consequence for humans would be dire (think a large spike in unemployment,
and starvation). Researchers have been able to narrow down CCD to factors such
as N. ceranae, but the mechanisms of how it was able to jump, or how it
changes protein expression is still in question. By putting effort into
unraveling these mysteries scientists in the future may be able to predict, or
even prevent such a future disaster. If that is still unsatisfacotry consider
this final point: should the garden variety A. mellifera go extinct the replacement
of choice would be a particular subspecies that has been so far no affected by
CCD. It's common name is simply the Killer Bee. And that dear reader is a world
I shudder to live in.

No comments:

Post a Comment

About Us

This blog represents the work of students from one of the few courses devoted to Eukaryotic Microbiology as a whole. This is a new experiment for this course that we hope will be a successful fusion of student learning and science communication. Enjoy, but play nice, comments are welcome but mean-spirited comments will be deleted.